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At least 919 records · Page 51Linked to original sources
PubMed1992

Skeletal muscle blood flow abnormalities in rats with a chronic myocardial infarction: rest and exercise.

The purpose of this study was to determine the regional distribution of blood flow deficit in the skeletal muscle vascular bed of rats with a chronic myocardial infarction (MI) and heart failure (HF). Accordingly, blood flow was determined (via radioactive microspheres) in rats with a small infarction (MI less than 30%) and in rats with a large (MI greater than 30%) infarction, induced by surgically ligating the left main coronary artery, and compared with rats that had received a sham operation. Results demonstrate that blood flow to the hindlimb musculature was significantly (P less than 0.05) less during a given level of treadmill exercise (20% grade and speed of 28 m/min) in the MI groups of rats compared with their sham counterparts. These differences in hindlimb blood flow were the result of blood flow deficits found in the individual muscles of the thigh and leg. Moreover, the blood flow deficits were more pronounced in the MI greater than 30% group of rats compared with the MI less than 30% group. The blood flow deficits found for the MI greater than 30% group of rats were positively correlated with the percentage of fast-twitch oxidative-glycolytic fibers and negatively correlated with the percentage of fast-twitch glycolytic fibers found in the individual muscles. Our study supports the contention that MI rats demonstrate skeletal muscle blood flow abnormalities during exercise. It appears that the degree of blood flow abnormalities produced in rats is dependent on the size of the MI and the amount of left ventricular dysfunction produced in the HF state.

Abdomen↗
PubMed1993

[Skeletal and respiratory muscle strength in chronic heart failure].

BACKGROUND: The aim of this study was to investigate limb and respiratory muscle strength in chronic heart failure (CHF). METHODS: Our study population consisted of 45 male CHF patients, 25 in NYHA Class II and 20 in NYHA Class III, and 22 male post-MI patients without left ventricular dysfunction (LVEF > 50%). All patients underwent assessment of respiratory muscle strength by maximal inspiratory (MIP) and expiratory (MEP) pressures, of handgrip force and peak torque developed during isokinetic Knee extension (EX) (quadriceps) and flexion (hamstring) at 120 degrees/sec. RESULTS: CHF patients showed a significant decrease in all limb and respiratory muscle strength compared to control patients. Moreover, NYHA Class III patients showed significantly reduced values of MIP, handgrip, and EX forces, as well as significantly reduced exercise tolerance in terms of METS (2.8 +/- 0.9 vs 4.4 +/- 1.2, p < .05) and anaerobic threshold level (9.4 +/- 3 vs 12.8 +/- 1.7 mlO2/Kg, p < .05), as compared to those patients in NYHA Class II, while no significant differences were observed in LVEF, cardiac index and pulmonary capillary wedge pressures. Weak, but significant (p < .05) were the correlations between limb muscle and respiratory muscle strength. No correlations were found between muscle force and hemodynamic parameters. Significant correlations (from p < .05 to p < .0001) were found among exercise tolerance and limb muscle strength, but not between exercise tolerance and respiratory muscle strength. In summary: 1) respiratory and skeletal muscle strength is impaired in CHF; 2) respiratory and limb muscle strength reductions are partially related to each other; 3) the degree of central hemodynamic impairment is not correlated with muscle force. Deconditioning could be a major determinant of skeletal but not respiratory muscle weakness. Other factors link limb and respiratory weakness in CHF.

Adult↗
PubMed1998

Characterization of the mitochondrial DNA abnormalities in the skeletal muscle of patients with inclusion body myositis.

Inclusion body myositis (IBM) is a late-onset inflammatory myopathy with distinctive clinical and histopathological features. The molecular basis for the disease remains unknown, but abnormal nuclear morphology and the accumulation of a protein that binds single-stranded DNA in a sequence-independent fashion suggest a nuclear defect. Evidence of mitochondrial respiratory chain dysfunction (ragged-red fibers, multiple mtDNA deletions) has been reported in IBM muscle. Here we have investigated the relationship of the mtDNA abnormalities in sporadic and familial IBM patients to the pathogenesis of the disease. In situ hybridization analysis with mtDNA probes revealed several different mtDNA abnormalities in cytochrome c oxidase-negative muscle fibers including large-scale mtDNA deletions and mtDNA depletion, but no evidence for nonspecific DNA binding. Contrary to previous reports, we did not observe mtDNA deletions on Southern blot analysis, consistent with the presence of multiple different deleted mtDNA species demonstrated by single fiber PCR. There was no consistent correlation between the mitochondrial abnormalities and markers of muscle regeneration, inflammation, or microscopically detectable pathological alterations of myonuclei in the same fibers. Thus, early molecular abnormalities in IBM may simply accelerate the accumulation of mtDNA abnormalities that occurs with natural aging.

Adult↗
PubMed1976

Iron deficiency in the rat. Physiological and biochemical studies of muscle dysfunction.

Work performance on a treadmill has been evaluated in normal and iron-deficient rats. Anemia was removed as a variable by adjusting the hemoglobin of all animals to the same concentration. At a hemoglobin compatible with normal work performance, iron-deficient animals showed a marked impairment of running ability as compared to control animals. Iron therapy corrected the disability within 4 days. Concentrations of the cytochrome pigments and myoglobin, and rates of oxidative phosphorylation with pyruvate-malate, succinate, and alpha-glycerophosphate as substrates were all reduced in mitochondrial preparations from skeletal muscle of iron-deficient rats, but only the rate of phosphorylation with alpha-glycerophosphate as substrate increased significantly and in parallel with the recovery in work performance of the iron-deficient rats treated with iron dextran.

Anemia, Hypochromic↗
PubMed2004

Mitochondrial respiratory chain dysfunction in ageing; influence of vitamin E deficiency.

The causes and consequences of ageing are likely to be complex and involve the interaction of many processes. It has been proposed that the decline in mitochondrial function caused by the accumulation of oxidatively damaged molecules plays a significant role in the ageing process. In agreement with previous reports we have shown that the activities of NADH CoQ1 reductase and cytochrome oxidase declined with increasing age in both rat liver and gastrocnemius muscle mitochondria. However, only in the liver were the changes in lipid peroxidation and membrane fluidity suggestive of an age-related increase in oxidative stress. After 12 weeks on a vitamin E deficient diet, vitamin E levels were undetectable in both gastrocnemius muscle and liver. In skeletal muscle, this was associated with a statistically significant increase in lipid peroxidation, a decrease in cytochrome oxidase activity after 48 weeks, and an exacerbation in the age-related rate of decline of NADH CoQ1 reductase activity. This was consistent with the suggestion that an imbalance between free radical generation and antioxidant defence may contribute to the mitochondrial dysfunction with age. In contrast to this, vitamin E deficiency in the liver caused a significant increase in mitochondrial respiratory chain activities with increasing age despite evidence of increased lipid peroxidation. Comparison of other features in these samples suggested vitamin E deficiency; did not have a significant impact upon mtDNA translation; induced a compensatory increase in glutathione levels in muscle, which was less marked in the liver, but probably most interestingly caused a significant decrease in the mitochondrial membrane fluidity in muscle but not in liver mitochondria. These data suggest that while increased lipid peroxidation exacerbated the age-related decline in muscle respiratory chain function this relationship was not observed in liver. Consequently other factors are likely to be contributing to the age-related decline in mitochondrial function and specific stimuli may influence or even reverse these age-related effects as observed with vitamin E deficiency in the liver.

Aging↗
PubMed2001

Functional inactivation of the IGF-I and insulin receptors in skeletal muscle causes type 2 diabetes.

Peripheral insulin resistance and impaired insulin action are the primary characteristics of type 2 diabetes. The first observable defect in this major disorder occurs in muscle, where glucose disposal in response to insulin is impaired. We have developed a transgenic mouse with a dominant-negative insulin-like growth factor-I receptor (KR-IGF-IR) specifically targeted to the skeletal muscle. Expression of KR-IGF-IR resulted in the formation of hybrid receptors between the mutant and the endogenous IGF-I and insulin receptors, thereby abrogating the normal function of these receptors and leading to insulin resistance. Pancreatic beta-cell dysfunction developed at a relative early age, resulting in diabetes. These mice provide an excellent model to study the molecular mechanisms underlying the development of human type 2 diabetes.

Aging↗
PubMed2004

Supra-physiological membrane potential induced conformational changes in K+ channel conducting system of skeletal muscle fibers.

The effects of a supra-physiological membrane potential shock on the conducting system of the delayed rectifier K(+) channels in the skeletal muscle fibers of frogs were studied. An improved double Vaseline gap voltage clamp technique was used to deliver stimulation pulses and to measure changes in the channel currents. Our results showed that a single 4 ms, -400 mV pulsed shock can cause a reduction in the K(+) channel conductance and a negative-shift of the channel open-threshold. Following the Boltzmann theory of channel voltage-dependence, we analyzed the shock-induced changes in the channel open-probability by employing both two-state and multi-state models. The results indicate a reduction in the number of channel gating particles after the electric shock, which imply possible conformational changes at domains that gate the channels proteins. This study provides further evidence supporting our hypothesis that high intensity electric fields can cause conformational changes in membrane proteins, most likely in the channel gating system. These structural changes in membrane proteins, and therefore their dysfunctions, may be involved in the mechanisms underlying electrical injury.

Animals↗
PubMed1996

Motor neuron disease with parkinsonism.

OBJECTIVE: To report clinical characteristics of patients with combined features of parkinsonism and motor neuron disease (MND). DESIGN: Medical chart review. SETTING: University medical center. PATIENTS: Thirteen patients, identified by computer-assisted search, who had diagnoses of both parkinsonism and MND. RESULTS: Median age was 68 years. There were 7 men and 6 women. All had clinical and electrodiagnostic evidence of both upper and lower motor neuron degeneration. One or more clinical manifestations of parkinsonism were observed in all patients either before the diagnosis of MND (n = 2), at the time of initial evaluation (n = 10), or after the diagnosis of MND (n = 1). The median time from symptom onset to presentation was 18 months. Improvement was seen in 5 of the 11 patients treated with levodopa. Dementia and autonomic dysfunction were absent in all patients. Postmortem neuropathological evaluation, available in 1 patient, demonstrated degeneration of the substantia nigra with Lewy bodies, mild pallor of the medullary pyramids, and neurogenic atrophy of the skeletal muscle. CONCLUSION: The onset of MND and parkinsonism within a relatively short period in most of our patients favors a common pathogenic mechanism over coincidental occurrence of 2 unrelated diseases. In patients with MND, it is important to recognize signs of parkinsonism that levodopa might alleviate.

Aged↗
PubMed2003

Ethylmalonic acid inhibits mitochondrial creatine kinase activity from cerebral cortex of young rats in vitro.

Short-chain acyl-CoA dehydrogenase (SCAD) deficiency is an inherited metabolic disorder biochemically characterized by tissue accumulation of predominantly ethylmalonic acid (EMA) and clinically by neurological dysfunction. In the present study we investigated the in vitro effects of EMA on the activity of the mitochondrial (Mi-CK) and cytosolic (Cy-CK) creatine kinase isoforms from cerebral cortex, skeletal muscle, and cardiac muscle of young rats. CK activities were measured in the mitochondrial and cytosolic fractions prepared from whole-tissue homogenates of 30-day-old Wistar rats. The acid was added to the incubation medium at concentrations ranging from 0.5 to 2.5 mM. EMA had no effect on Cy-CK activity, but significantly inhibited the activity of Mi-CK at 1.0 mM and higher concentrations in the brain. In contrast, both Mi-CK and Cy-CK from skeletal muscle and cardiac muscle were not affected by the metabolite. We also evaluated the effect of the antioxidants glutathione (GSH), ascorbic acid, and alpha-tocopherol and the nitric oxide synthase inhibitor L-NAME on the inhibitory action of EMA on cerebral cortex Mi-CK activity. We observed that the drugs did not modify Mi-CK activity per se, but GSH and ascorbic acid prevented the inhibitory effect of EMA when co-incubated with the acid. In contrast, L-NAME and alpha-tocopherol could not revert the inhibition provoked by EMA on Mi-CK activity. Considering the importance of CK for brain energy homeostasis, it is proposed that the inhibition of Mi-CK activity may be associated to the neurological symptoms characteristic of SCAD deficiency.

Animals↗
PubMed1979

Radiography of glycogen storage diseases.

Sixty-three patients with glycogen storage disease were evaluated. Findings on plain film examinations, excretory urography, barium gastrointestinal studies, ultrasonography, and angiography were categorized by type of glycogen storage disease. In type I findings include hepatomegaly with hepatic dysfunction, renomegaly with an increased incidence of renal calculi, and osteopenia with various associated osseous abnormalities. These changes were less pronounced in types III, IV, and VI. Type II displayed either cardiac or skeletal muscle glycogen deposition. Correlation with postmortem examination in 14 individuals is given.

Adolescent↗
PubMed2004

Neuromuscular quadriceps dysfunction prior to osteoarthritis of the knee.

Decreased maximal quadriceps strength and voluntary activation has been observed in patients with osteoarthritis in previous studies, but those results do not allow any conclusions to be drawn as to whether quadriceps dysfunction precedes or follows osteoarthritis. Thirty-two patients (group a) who underwent partial meniscectomy 48+/-9 month prior to the study were matched according to their weight and body mass index with a control group (group b). The twitch interpolation technique was used to determine maximal voluntary contraction (MVC) and voluntary activation (VA) of the quadriceps muscle of both legs. Subjective assessment of the knee was performed using the Lysholm-Score. AP and lateral X-rays of the operated knee were obtained. None of the participants showed any evidence of characteristic radiological or clinical signs for osteoarthritis. A significantly lower MVC was noticed in both the affected and the contralateral knee of group a in comparison to group b (p < 0.01). The VA in group a yielded 80.9+/-15.4% for the injured side and 83.1+/-11.5% for the contralateral side, with no statistical difference (p = 0.18). The VA in group b was 89.4+/-5.8% for the right side and 88+/-6.8% for the left side both being significantly higher in comparison to group a. This study has shown, that patients following meniscus resection present with bilateral quadriceps weakness as already described in patients with manifest osteoarthritis. The authors hypothesise that muscle dysfunction may be an etiologic factor underlying the pathologic changes of osteoarthritis. Whether muscle dysfunction occurs also at other sites, e.g. in the upper extremity, remains unclear but would be of interest in order to detect a generalized neuromuscular dysfunction.

Adult↗
PubMed1998

Postural control in sitting children with cerebral palsy.

Children with cerebral palsy (CP) display postural problems, largely interfering with daily life activities. Clarification of neural mechanisms controlling posture in these children could serve as a base for more successful intervention. Studies on postural adjustments following horizontal forward and backward displacements of a movable platform in ten school-age children with spastic diplegia and non-disabled controls revealed that sitting CP children, like standing CP children, show direction specific postural adjustments, indicating that the basic pattern of muscle coordination in these conditions is conserved. Dysfunctions are especially present in the modulation of the response pattern of ventral muscles during forward translations. They consist of: (1) a stereotyped and non-variable activation of all ventral muscles; (2) an abnormal top-down muscle recruitment; and (3) an excessive degree of antagonistic co-activation. The altered patterns of muscle coordination could be the result of two interacting mechanisms, the primary deficit due to the early brain damage and a compensation due to the postural instability. Especially the latter dysfunction furnishes opportunities for therapeutic help.

Cerebral Palsy↗
PubMed1998

Ultrastructural abnormality of sarcolemmal nuclei in Emery-Dreifuss muscular dystrophy (EDMD).

We performed ultrastructural studies on nuclear abnormalities in biopsied muscles from seven patients with EDMD, of three non-related families, and two sporadic cases. The diagnosis was based on clinical data and molecular findings. We detected different degrees of abnormalities in the sarcolemmal nuclei ranging from marked condensation of chromatin to complete damage of nuclear components. Other nuclei in the same muscle cell very often appeared normal. The extrusion of nuclear chromatin into sarcoplasm as a consequence of nuclear membrane disintegration was observed in numerous nuclei. All these nuclear changes are considered to be cytological indicators of nuclear dysfunction evoked by emerin deficiency.

Cell Nucleus↗
PubMed2001

Anatomical variations of the scalene triangle: dissection of 10 cadavers.

STUDY DESIGN: Cadaver dissection to study the anatomy of the scaleni muscles and surrounding structures. OBJECTIVES: To analyze in depth the anatomy of the scaleni muscles and surrounding structures, and to further document anatomical variations which have been reported in the literature. BACKGROUND: The literature reported variations in the attachments of the scaleni muscles, as well as the presence of a scalenus minimus muscle. The importance of these muscles in the respiratory and musculoskeletal systems led us to study these muscles with dissection. METHODS AND MEASURES: We performed anatomical dissection on 10 cadavers. The findings from the cadavers were analyzed and reported. RESULTS: The attachments of the 3 primary scaleni muscles (anterior, medius, and posterior) were variable. The actual width of the scaleni muscles (anterior, medius, and posterior) at the C6 tubercle and at the first rib also varied. A scalenus minimus was present in one cadaver and presumably present in 2 others. The scalenus anterior muscle arose in 20% of the specimens from C3 to C6, in 30% of the specimens from C3 to C7, in 20% of the specimens from C4 to C5, and in 30% of the specimens from C4 to C6. The scalenus anterior muscle arose from C3 in 50% of the dissections. An attachment to C7 was observed in 30% of the cadavers. The widths of the scalenus anterior muscles at their insertion were between 8 and 17 mm. The scalenus medius muscle arose in 40% of the specimens from C2 to C6. In 60% of the cadavers, the scalenus medius muscle had an attachment to C7. Fifty percent of the scalenus medius muscles arose from C2 and 50% also had an origin from C1. The widths of the scalenus medius muscles at their insertion were between 10 and 20 mm with a mean of 15.5 mm. Fifty percent of the scalenus posterior muscles arose from C4 to C6 and 50% arose from C5 to C6. CONCLUSIONS: Variations were found in the attachments and the size of the scaleni muscles. These variations may effect the size of the scalene triangle, and thus, may potentially result in varied signs and symptoms in patients who have cervical, thoracic, and rib dysfunctions. Clinical implications were postulated.

Cadaver↗
PubMed2004

Transcatheter transplantation of autologous skeletal myoblasts in postinfarction patients with severe left ventricular dysfunction.

PURPOSE: To report a case-controlled safety and feasibility study of transcatheter transplantation of autologous skeletal myoblasts as a stand-alone procedure in patients with ischemic heart failure. METHODS: Six men (mean age 66.2+/-7.2 years) were eligible for transcatheter transplantation of autologous skeletal myoblasts cultured from quadriceps muscle biopsies. Six other men (mean age 65.7+/-6.3 years) were selected as matched controls (no muscle biopsies). A specially designed injection catheter was advanced through a femoral sheath into the left ventricle cavity, where myoblasts in solution (0.2 mL/injection) were injected into the myocardium via a 25-G needle. At baseline and in follow-up, both groups underwent Holter monitoring, a 6-minute walk test, New York Heart Association (NYHA) class determination, and echocardiography with dobutamine challenge. RESULTS: Skeletal myoblast transplantation was technically successful in all 6 patients with no complications; 19+/-10 injections were performed per patient (210 x 10(6)+/-150 x 10(6) cells implanted per patient). Left ventricular ejection fraction (LVEF) rose from 24.3%+/-6.7% at baseline to 32.2%+/-10.2% at 12 months after myoblast implantation (p=0.02 versus baseline and p<0.05 versus controls); in matched controls, LVEF decreased from 24.7%+/-4.6% to 21.0%+/-4.0% (p=NS). Walking distance and NYHA functional class were significantly improved at 1 year (p=0.02 and p=0.001 versus baseline, respectively), whereas matched controls were unchanged. CONCLUSIONS: Transcatheter transplantation of autologous skeletal myoblasts for severe left ventricular dysfunction in postinfarction patients is feasible, safe, and promising. Scrutiny with randomized, double-blinded, multicenter trials appears warranted.

Aged↗
PubMed1999

Blood loss in Duchenne muscular dystrophy: vascular smooth muscle dysfunction?

Patients with Duchenne muscular dystrophy (DMD) tend to bleed more during surgery than do patients with other conditions. A retrospective analysis of blood loss after spinal surgery for scoliosis was therefore undertaken in 102 patients undergoing surgery in the senior author's unit. These included 48 patients with DMD, 26 patients with spinal muscular atrophy, and a miscellaneous group of 28 other patients most of whom had idiopathic scoliosis. For each patient the age at surgery, estimated blood volume, duration of operation, Cobb angle, and number of vertebrae fused were recorded and compared. Expression of dystrophin in skeletal muscle and the underlying gene mutation were also determined. The estimated blood loss in patients with DMD was significantly higher than that in patients with spinal muscular atrophy undergoing the same or similar procedure (P < 0.005) and was also significantly greater than that of the third group, which consisted mostly of patients with idiopathic scoliosis (P < 0.0005). Blood loss in the patient group with DMD showed a significant relationship with duration of surgery (P < 0.05). As most patients expressed no dystrophin, this did not correlate with the estimated blood loss. There was also no correlation between the estimated blood loss and the type of gene mutation found causing DMD. The authors' previous observations confirm the increased blood loss in patients with DMD who undergo scoliosis surgery. Because children with DMD lack dystrophin in all muscle types, including smooth muscle, the excessive blood loss may be because of a poor vascular smooth muscle vaso-constrictive response due to a lack of dystrophin.

Adolescent↗
PubMed2007

[The influence of somatic dysfunction on chronic muscular skeletal pain syndromes].

Chronic muscular skeletal pain syndromes (CMSPS) are one of the major health issues. Despite progress in research, treatment and diagnosis remain difficult. The aim of this study was to examine the influence of somatic dysfunction on CMSPS. A total of 216 patients were examined in a standardized way to assess the influence of morphological and psychosocial factors as well as of somatic dysfunction on CMSPS. Measurements were taken at admission. The results showed a statistically significant link between somatic dysfunction, pain chronicity, pain distribution, and pain-related disability. Since there was no or only a minor correlation between somatic dysfunction and the results of the psychometric testing and the morphological findings, somatic dysfunction should be regarded as an independent factor influencing CMSPS and be further scientifically evaluated.

Chronic Disease↗